Category: 8. Health

Characterization and relatedness of the isolates

The susceptibility profiles of six clinical A. pittii isolates are presented in Table 1. All isolates were susceptible to aminoglycosides, tetracyclines and fluoroquinolones. All isolates were susceptible to ceftolazone/tazobactam, colistin, ampicillin/sulbactam, trimethoprim/sulfamethoxazole and nitrofurantoin; and resistant to ampicillin, first generation cephalosporin cefazolin, 3rd generation cephalosporins ceftriaxone and cefotaxime and aztreonam. Two isolates (AP290R and AP5092) were intermediate to piperacillin/tazobactam and resistant amoxicillin/clavulanic acid; only one isolate (AP290R) was resistant to all carbapenems tested and had elevated levels of ceftazidime (8 ug/ml).

The six A. pittii isolates and reference strain ATCC19606 were analyzed by FT-IR to determine phenotypic similarity. No clusters (indicating similar isolates) were evident (Fig. 1A). To determine whether FT-IR could distinguish between A. pittii and A. baumannii, we added 11 A. baumannii strains, belonging to different sequence types (STs), to the FT-IR analysis. Still no clusters were identified, and A. pittii isolates were not always more similar to each other than to A. baumannii isolates (Fig. 1B).

All 6 A. pittii strains were sequenced and their genomes were analyzed. The isolates belonged to different STs (Table 2) with different KL types. We constructed a phylogenetic tree based on pangenome analysis (Supplementary Fig. 1). The tree revealed distinct separation, with consistent and even distances observed between each isolate. Next, we conducted core genome alignment of the six A. pittii isolates compared to 64 publicly available complete genomes of A. pittii (Supplementary Table 1) from different countries and different years. The genomes represent a temporal range spanning from 2011 to 2024, allowing for examination of potential genomic changes over nearly three decades. This analysis placed AP5092 and MML4 (isolated in 2023, Hong Kong) on one branch close to each other. Other four isolates were located on a second branch, with AP5047 and AP290R most closely related to each other (Fig. 2). Isolate AP290R most close to isolate HCG18 isolated in Mexico in 2023.

Antibiotic resistance genes

Genomic analysis revealed the presence of several antimicrobial resistance determinants among the isolates (Table 3).

All isolates carried at least two genes conferring β-lactam resistance: a variant of ampC cephalosporinase (ADC) and a variant of OXA-type β-lactamase. Notably, isolate AP290R carried three bla_OXA genes – bla_OXA−272, bla_OXA−255 and bla_OXA−72 carbapenemases. Correspondingly, this was the only isolate to display carbapenem resistance.

In addition, all six study isolates harbored genes conferring quinolone resistance (adeF and abaQ), efflux pump components (abeS, adeF and adaQ), and a gene involved in colistin resistance (lpsB). Three isolates (AP4773, AP4968, and AP5092) contained a single putative aminoglycoside resistance gene, ant(3’’)-IId, with relatively low sequence homology (69%) to the closest match in the Comprehensive Antibiotic Resistance Database (CARD).

Virulence studies

In vitro phenotype

We next evaluated characteristics of the A. pittii isolates which are classically associated with bacterial virulence – growth, motility and biofilm formation. A. baumannii reference strain ATCC19606 served as a reference strain. The growth of all isolates was similar to that of the control strain (p > 0.05; Supplementary Fig. 2). Three A. pittii isolates demonstrated significantly higher motility than the control stain (p < 0.0001) (Fig. 3A), and four isolates produced significantly less biofilm (p < 0.001) (Fig. 3B).

All A. pittii isolates were serum sensitive (Fig. 3C), displaying either death (4/6 isolates) or reduced growth (2/6 isolates) after 4 h exposure to NHS. Heat inactivation of the complement system reduced the serum sensitivity of 5/6 isolates (except for AP5091), with one isolate (AP5092) displaying full resistance to the inactivated serum.

In vivo virulence

We next evaluated the virulence of the A. pittii isolates in vivo, using killing assay in Z. morio larvae. In this model, AP290R exhibited high virulence potential (Fig. 4), killing 70% of infected Z. morio larvae within 24 h. The other A. pittii strains were less lethal, with a 10%−20% lethality rate 24 h post infection and a 25%−35% lethality rate 7 days post infection.

Virulence factors

AP290R possessed the largest number of virulence genes, and AP4773 and AP5092 – the smallest. Nine virulence genes (cpaA, entE, gspDE1E2FINO, bauCDF, pilBCFGHMTU2D, pbpG, lpxABCL, barB, lbsB) were present in all 6 isolates (Fig. 5). These genes are related to various virulence functions, including biofilm formation, adherence, coagulation (cpaA), siderophore biosynthesis (entE), motility, and others. Several differences in genomic content were evident. The cluster of three genes – pilA, pilQ (surface motility) and basI (siderophore biosynthesis) – was missing from AP290R, AP4773, AP4968 and AP5091. However, only pilA was missing in isolate AP5092, and only basI was missing in isolate AP5047. The iron acquisition gene barA was missing in AP5047.

Plasmid content

Whole genome analysis revealed that two A. pittii isolates carried plasmids. Properties of these plasmids are described in Table 4 and the specific ORFs – in Supplementary Table 3. Plasmid p290R (Fig. 6A) carried ten hypothetical proteins and 4 genes of known function: ydhP (associated with glycosidase and hydrolase activity), azoR1 (azoreductaze), gcvA (regulates the glycine cleavage system, transcriptional activator), and most significantly – the carbapenemase bla_OXA−72 gene. The much larger plasmid p5092 (Fig. 6C) carried 119 genes, among them genes involved in different metabolic pathways, transporters and transcriptional regulators, and several insertion sequences (ISAba46, ISAba22, ISAba23, ISAha3, ISAcsp3, ISAba26 and IS1301), and 79 hypothetical proteins.

BLASTn analysis revealed a significant number of comparable plasmids within the public database, all reported in Acinetobacter spp. From this pool, we selected the ten most closely related plasmids for each of the plasmids (pAP5092 and pAP290R) and constructed a phylogenetic tree (Fig. 6B, D). The plasmid closest to pAP290R was pSU8507_OXA-2 (accession number LC777725.1) isolated from A. pittii in Japan in 2023, followed by 5 closely related plasmids from the US, China and Spain isolated in 2017–2021 (Fig. 6B). The plasmid closest to pAP5092 found in the database was pML4_1 (accession number CP118934.1) isolated from A. pittii in Hong Kong in 2023 (Fig. 6D). Additional information regarding accession numbers, year and country of isolation can be found in Supplementary Table 2.

Plasmid pAP290R contained the bla_OXA−72 gene (an OXA-24 family carbapenemase). To test the inter-species transferability of this plasmid, it was extracted from A. pittii AP290R and electroporated it into AB2142, a carbapenem-susceptible A. baumannii strain. Plasmid pAP290R conferred resistance to beta-lactams and carbapenems (Supplementary Tables 4 and Supplementary Fig. 3). However, resistance to ceftazidime in AP290R seems to be intrinsic; it was not transferred to AB2142 by the pAP290R plasmid.

Crucially, the plasmid also significantly increased the virulence of AB2142 (Fig. 7), suggesting that it contributes to the virulence of AP290R, raising the possibility that some of the hypothetical genes it carries are in fact virulence factors.

The diagnosis of chronic obstructive pulmonary disease, or COPD, is improved by incorporating CT lung imaging and respiratory symptoms. This fresh, multidimensional approach better identifies patients who are at risk of poor respiratory outcomes, while ruling out those who have airflow obstruction without respiratory symptoms or structural lung disease, Surya Bhatt, M.D., and colleagues report in the Journal of the American Medical Association.

This new COPD diagnostic schema, which includes chest imaging, respiratory symptoms and spirometry, identified additional individuals at risk of poor respiratory outcomes.”

Surya Bhatt, M.D., professor, Department of Medicine, University of Alabama at Birmingham Marnix E. Heersink School of Medicine and director, Center for Lung Analytics and Imaging Research

The schema includes airflow obstruction on spirometry as the major criterion and minor criteria based on chest imaging and respiratory symptoms. Imaging includes visual signs of emphysema and airway wall thickening on computed tomography, and symptom-based criteria consider difficulty breathing, reduced quality of life and the presence of chronic bronchitis. Under the new framework, a patient must have airflow obstruction and at least one minor criterion or, in the absence of airflow obstruction or if lung function tests are not available, at least three of five minor criteria.

Bhatt and colleagues found that, among 9,416 participants enrolled in a multicenter cohort, those newly diagnosed with COPD by the schema had greater all-cause and respiratory-specific mortality, more frequent exacerbations, and faster lung function decline compared with people classified as not having COPD based on the new classification. This new diagnostic schema included additional individuals with high respiratory morbidity and excluded some with airflow obstruction who had no symptoms or evidence of structural lung disease.

Before this study, clinicians had increasingly recognized that lung function tests did not capture all aspects of the complex heterogeneous disease COPD, a leading cause of disability and death. Some 392 million people globally, and 16 million in the United States, are estimated to have COPD.

“This new diagnostic schema will likely change the way we diagnose COPD and enable its diagnosis, even in the absence of overt airflow obstruction on spirometry,” Bhatt said. “Whether treating individuals newly diagnosed this way will result in improved outcomes remains to be tested, but practitioners have already been using imaging and symptoms to diagnose COPD. This new schema sets some parameters to operationalize this.”

In an editorial in JAMA, Francesca Polverino, M.D., Ph.D., called the study a milestone in COPD diagnosis. “COPD classification has remained overly dependent on airflow limitation as the main diagnostic criterion,” Polverino wrote. “What truly sets this reclassification apart is its groundbreaking assertion that airflow obstruction is no longer a requirement for a COPD diagnosis.”

In the system proposed by Bhatt and colleagues, airflow obstruction remains the major criterion for COPD. “However, what makes this model significantly more inclusive and reflective of clinical COPD diversity are the minor criteria, which are split between imaging and symptom-based factors,” said Polverino, a professor at the Baylor College of Medicine, Houston, Texas.

Bhatt is corresponding author of the study, “A new multidimensional diagnostic approach for chronic obstructive pulmonary disease,” and Edwin K. Silverman, M.D., Ph.D., Brigham and Women’s Hospital, Boston, Massachusetts, and James D. Crapo, M.D., National Jewish Health, Denver, Colorado, are co-senior authors. Other UAB authors include Mark Dransfield and Sandeep Bodduluri, UAB Department of Medicine Division of Pulmonary, Allergy and Critical Care Medicine; and Arie Nakhmani, UAB School of Engineering Department of Electrical and Computer Engineering.

The study includes 52 authors from 24 universities and institutions in the United States and Canada.

At UAB, Bhatt works in the Division of Pulmonary, Allergy and Critical Care Medicine.

Source:

University of Alabama at Birmingham

Journal reference:

Bhatt, S. P., et al. (2025). A Multidimensional Diagnostic Approach for Chronic Obstructive Pulmonary Disease. JAMA. doi.org/10.1001/jama.2025.7358.

When it comes to matters of life and death, could human survival depend on our mastery of game strategy?

For biologists, evolutionary game theory is a way of studying how different traits or behaviors evolve in a population over time, impacting the probability of a population’s survival in relation to the strategies present in other competing populations. This creates a constantly shifting balance – comparable to a dynamic and ever-changing version of rock-paper-scissors – in which strategy is a matter of timing and knowing your opponent.

A research team led by Paul Newton, professor of aerospace and mechanical engineering, mathematics, and quantitative and computational biology at USC Viterbi School of Engineering, has published a new paper in PNAS demonstrating how principles of game theory can be applied to advance cancer therapy.

The authors of the paper have developed a mathematical model that taps into the dynamics of the cancer-immunity cycle, predicting the competition of cancer cells, healthy cells, and immune system cells (T-cells). The insights developed from the model have the potential to allow medical practitioners to effectively “game” the cycle – synchronizing treatment schedules based on the battles taking place in the human body.

“You can think of a tumor as an ecosystem consisting of cancer cells competing with healthy cells,” said Newton. “Chemotherapy and immunotherapy are essentially attempts to steer the evolution of the tumor in a beneficial way. But that’s not how oncologists have typically framed approaches to treatment.”

The new paradigm proposed by the paper will seem shocking to some – after all, we’re used to thinking in terms of eliminating cancer cells, not trying to get the tumor on our side. The trouble is, the elimination method rarely works; the cells that are most sensitive to the chemotherapy will be killed off, while those that have developed resistance via mutations will survive. Those resistant cells regrow, leading to cancer recurrence.

“The motivation of our model is to develop an evolutionary game theory model which incorporates this selection dynamics of these competing cell populations,” said Newton. “Of course, we want to reduce the size of the tumor by killing some of the sensitive cells – but if you kill all of them, then the resistant cells are going to take over.”

As war games go, this is among the more complex. The immune system is an ally that requires careful management, as T cell populations start to attack the cancer cells and shape the rise and decline of different subpopulations of cells. In Newton’s framework, cancer cells act as defectors in a population dynamics game, while healthy cells act as cooperators, and the immune system serves as a dynamic regulator that modulates the rules of the game through feedback.

“Our thinking about the cyclical process of how cancer cells interact with T cells was influenced by Daniel S. Chen and Ira Mellman’s influential paper ‘Oncology meets immunology: the cancer-immunity cycle,’” Newton explained. “We set out to ask a series of important questions that build upon this foundation. What are the benefits of synchronizing chemotherapy and immunotherapy schedules with the cycle, as predicted by mathematical modelling? And could this strategic timing of treatment enable lower doses with the same – or greater – positive impact as standard doses?”

The work conducted by Newton’s team represents one of the first comprehensive mathematical models to treat the cancer-immunity cycle as a dynamic, game-theoretic system. If validated in patient populations, the findings could reshape how oncologists schedule combination therapies – not just based on standard cycles or tolerance, but on personalized biological rhythms.

Measuring the exact period of a patient’s cancer-immunity cycle remains a challenge. But advances in real-time immune-monitoring – via circulating tumor DNA, immune profiling, or imaging – may soon make it possible. Newton’s team envisions future clinical protocols that use sparse data collection and statistical inference to approximate the cycle and adjust therapy in real time. “We’re not just fighting cancer we’re negotiating with it,” said Newton. “And timing is everything.”

Published on August 12th, 2025

Last updated on August 12th, 2025

First introduced in 1881 by Austrian-Jewish physician Samuel Siegfried Karl von Basch, and brought into broad U.S. use at the turn of the 20th century by neurosurgeon Harvey Cushing, M.D., the inflatable cuff, or sphygmomanometer, has changed little in more than a century.

Now, University of Cambridge researchers say the familiar test may be missing thousands, even millions, of cases of high blood pressure.

Published August 12 in PNAS Nexus, a new study reveals a physical quirk in the gold-standard auscultatory method that can cause systolic pressure readings to register lower than they really are. As a result, as many as 30% of patients with systolic hypertension could go undiagnosed.

High blood pressure — a leading risk factor for premature death — often shows no symptoms until serious complications strike. That makes accurate readings essential.

The physics behind the error

In the auscultatory method, the cuff inflates around the upper arm to stop blood flow. As it deflates, clinicians listen for Korotkoff sounds — the telltale taps that signal blood is once again moving through the artery — to determine systolic and diastolic pressures.

While overestimation of diastolic pressure is well understood, underestimation of systolic pressure has been harder to explain.

“We have a good understanding of why diastolic pressure is overestimated,” said co-author Kate Bassil, of the University’s engineering department. “But why systolic pressure is underestimated has been a bit of a mystery.”

Using a custom-built model, the team showed that when the cuff fully closes the artery, pressure in the vessels downstream drops to a steady, low level. This low pressure delays the artery’s reopening as the cuff deflates, meaning the first Korotkoff sound — and the systolic reading — comes later than it should.

Meta-analyses indicate that cuff-based devices can underestimate systolic blood pressure by close to 6 mmHg on average, which is enough to miss roughly one in three cases of systolic hypertension.

Because automated devices are validated against manual auscultatory measurements, the same error often carries over to newer technologies.

“Pretty much every clinician knows blood pressure readings are sometimes wrong, but no one could explain why they are being underestimated — there’s a real gap in understanding,” said co-author Anurag Agarwal, a professor in Cambridge’s Department of Engineering.

What’s the fix?

Researchers say the solution might be as simple as adjusting technique.

One promising option: raising the patient’s arm before inflating the cuff. This simple step reduces venous pressure in the limb, creating a more predictable downstream pressure. Because the degree of underestimation is tied to downstream pressure, having a consistent, known value makes it easier to adjust the reading accurately.

Plus, the change wouldn’t require any new equipment, only a slight modification to the existing auscultatory protocol.

In practice, it could be combined with a short rest period before measurement to stabilize pressures and ensure repeatability.

For longer-term improvements, the team envisions integrating correction factors directly into blood pressure devices. New or updated models could use patient-specific data — age, arm circumference, body mass index or pulse wave velocity — to estimate downstream pressure and automatically adjust systolic readings in real time.

“You might not even need new devices, just changing how the measurement is done could make it more accurate,” said Agarwal.

A medication developed in the 1950s to treat Parkinson’s disease may offer a powerful new tool in the fight against tuberculosis (TB), according to new research from the University of British Columbia.

Published in npj Antimicrobials & Resistance, the study found that benztropine, a drug used to manage tremors in patients with Parkinson’s, can dramatically reduce levels of TB-causing bacteria by boosting the body’s natural immune response.

TB is the world’s deadliest infectious disease, typically affecting the lungs and causing an estimated 1.3 million deaths each year. Treatment requires a months-long regimen of multiple antibiotics, which can have serious side effects and is increasingly challenged by the emergence of drug-resistant bacterial strains.

New approaches for treating tuberculosis are urgently needed. By enhancing immune function rather than targeting the bacteria, this could be a powerful tool against drug-resistant TB. And, it’s a compound that has already proven safe in people with Parkinson’s.”

Dr. Yossef Av-Gay, senior author, professor of infectious diseases, UBC faculty of medicine

Tuberculosis is particularly difficult to treat because the bacteria responsible, Mycobacterium tuberculosis, is able to infect and survive within the very immune cells designed to destroy pathogens, known as macrophages.

While antibiotics work by killing the bacteria directly, benztropine functions through an alternative approach that supercharges immune cells to fight back. The drug blocks a receptor on macrophages that TB bacteria exploit, allowing the cells to regain their ability to kill the bacterial invaders.

The researchers say treatments that enhance the body’s natural defences, known as host-directed therapies, could offer significant benefits in the fight against TB.

“Because these therapies don’t directly target the bacteria, they’re far less likely to drive drug resistance,” said lead author Dr. Henok Sahile, a postdoctoral researcher in UBC’s faculty of medicine. “They can also work in combination with existing antibiotics to improve treatment outcomes or help in cases where antibiotics fail.”

To identify benztropine, the research team screened a library of more than 240 U.S. Food and Drug Administration-approved drugs by testing each compound on immune cells infected with TB.

Benztropine emerged as a standout candidate, capable of significantly reducing TB bacterial counts in experiments with both human and mouse immune cells. The researchers then tested benztropine in mice infected with TB, with oral treatment leading to a 70 per cent reduction in bacterial load in the lungs-comparable to some current TB treatments.

The drug showed similar effectiveness in a separate mouse model of Salmonella infection, suggesting its potential as a treatment for a wide range of pathogens.

Because benztropine is already approved for use in humans, the researchers say the findings could accelerate its path to clinical testing for TB and other infections.

“Repurposing existing drugs is one of the fastest and most cost-effective ways to bring new treatments to patients,” said Dr. Av-Gay. “With benztropine, we already understand the safety profile and pharmacology, which means we can move more quickly toward clinical trials.”

The interdisciplinary research team involved microbiologists, immunologists and infectious disease experts at UBC’s Life Sciences Institute, as well as collaborators at the Vaccine and Infectious Disease Organization at the University of Saskatchewan.

This study was supported by the Canadian Institutes of Health Research.

A new vaccine aimed at a common cancer gene mutation could help stop aggressive pancreatic cancers from coming back, a small clinical trial suggests.

Pancreatic cancer is one of the most lethal cancers, with a five-year survival rate of about 13%, according to the American Cancer Society.

Further, up to 80% of cases return after treatment, the National Institutes of Health says.

“If you were to ask me what disease most needs something to prevent recurrences, I’d say this one,” Dr. Zev Wainberg, a leader of the trial, told NBC News. He’s co-director of the University of California, Los Angeles gastrointestinal oncology program.

The experimental vaccine targets KRAS gene mutations, which are found in about 25% of all cancers, the University of Texas MD Anderson Cancer Center says. This includes up to 90% of pancreatic cancers and roughly 40% of colon cancers.

While these mutations have long been considered impossible to treat with drugs, researchers are finding new ways to target them.

The vaccine, called ELI-002 2P, uses small chains of amino acids called peptides to train the immune system to spot and destroy cells with KRAS mutations.

Unlike many cancer vaccines that are custom-made for each patient, this one is designed to be off the shelf, meaning it doesn’t require the tumor to be sequenced before it’s used, NBC News reported.

The Phase 1 study — reported Tuesday in Nature Medicine — included 20 people with pancreatic cancer and five with colon cancer. All had KRAS mutations and had already undergone surgery and chemotherapy.

Blood tests after surgery showed microscopic evidence of residual disease – cancer cells too small to see on scans. These leftover cells can cause the cancer to spread and return.

Post-surgery, participants received up to six priming doses of the vaccine, with 13 also getting booster shots. In all, the process took six months.

Here’s what the results showed:

85% (21 of 25 participants) had an immune response to the KRAS mutations.

About two-thirds of those had a strong enough response to help clear lingering cancer cells.

Nearly 70% developed immunity to other tumor targets not included in the vaccine.

A few “super-responders” had exceptionally strong immune reactions and the best outcomes.

In the pancreatic cancer group, patients survived for an average of 29 months, staying recurrence-free for more than 15 months after vaccination.

“That far exceeds the rates with resectable [surgically removable] cancers,” Wainberg said.

Cancer vaccines have been difficult to create because cancer cells share many proteins with healthy cells, making safe targets hard to find. Advances in mRNA technology and faster gene sequencing are now making more effective cancer vaccines possible.

The peptides in this vaccine also have a unique “tail” that helps them stay in lymph nodes, where immune cells are activated — a feature past peptide vaccines didn’t have, said Stephanie Dougan, an associate professor at Dana-Farber Cancer Institute in Boston, who was not involved in the study.

More research is needed to confirm the findings, and a Phase 2 trial is now underway to compare the vaccine with standard care.

“The fact that the long-term survival really correlated with T-cell response suggests that the vaccine caused this,” Dougan said, referring to the specific immune cells activated by the vaccine. “The idea that you can target KRAS is really exciting.”

More information

The Mayo Clinic has more on pancreatic cancer.

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As autism diagnoses continue to grow and remain a topic of nationwide debate, new research reveals that autistic individuals are facing mental health challenges at a major turning point in their lives – when they go to college.

According to a new study led by researchers at Binghamton University, State University of New York, autistic college students face dramatically higher rates of anxiety and depression compared to their non-autistic peers. 

Psychologists at Binghamton University examined data from the National Survey of Student Engagement (NSSE), which included 342 universities and 149,783 undergraduate student respondents. Of the questions posed, students can report being autistic and also whether or not they have a diagnosis of anxiety or depression. The researchers analyzed the data to determine the rate of anxiety and depression for those who also reported being autistic. 

What we found is really staggering – autistic individuals endorse much higher rates of anxiety and depression compared to their non-autistic peers.”

Diego Aragon-Guevara, lead author on the paper and PhD student in psychology at Binghamton

Aragon-Guevara, whose main research focus is improving the quality of life for autistic adults, said that autistic college students are an underrepresented, under-researched population.

“We wanted to sort of fill that gap in the research and find out how they are doing,” he said. “What are some challenges that they’re having, specifically around mental health, since mental health in college is really such an important topic,” he said. 

2021 marked the first year that autism was an endorsable category in the survey. According to paper co-author Jennifer Gillis Mattson, that added representation allows researchers to more readily conduct research on autistic students and compare them with their non-autistic peers. 

“We were really excited to see what the data would tell us. It was a big opportunity to be able to do this,” said Mattson, professor of psychology and co-director of the Institute for Child Development at Binghamton University. 

The study highlights the need for more mental health support for autistic students, said the researchers. 

“We want to provide the best support for them and to make sure that they have a college experience, where they get a lot out of it, but also feel comfortable,” said Aragon-Guevara.

For example, support personnel might address an individual’s autism and, in the process, overlook their mental health issues. More care needs to be put into addressing that nuance, said Gillis-Mattson.

“We’re shedding some light on the fact that if you have autistic college students in your college population – and we know the number of autistic college students continues to increase every single year – then we really do have an obligation to support these students,” said Gillis-Mattson. “And to know how best to support these students and we need to look beyond just autism, if you will. That there are these other mental health conditions, such as anxiety or depression, where people need to be able to acknowledge and understand that additional supports may be needed.”

Aragon-Guevara said that this new research is a starting point – confirmation that there is an issue regarding mental health in autistic college students. The researchers next want to identify the specific factors that influence these mental health challenges, whether it’s social dynamics, support from faculty, accessibility, etc. 

“There are so many elements that go into being comfortable in the new environment that is college, so we want to look into that and see if there are any deficits in those areas that autistic college students are experiencing, so that we know where we can help support them, or create institutional things to help improve quality of life as a whole,” said Aragon-Guevara.

This study is part of a broader research effort at Binghamton to better understand and support autistic students in higher education. Hyejung Kim, an assistant professor in the Department of Teaching, Learning and Educational Leadership, noted that there is still much to explore about this population. 

“This population often skews male, and interactions between personal factors and conditions such as anxiety and depression may shape overall well-being in college, an area that warrants further study,” she said. “Autistic students are also more likely to pursue STEM fields, and many report different experiences with faculty and staff across institutional settings. We still have much to learn about how these and other contextual factors relate to mental well-being.” 

The research team plans to examine these factors more closely, in collaboration with campus partners, to inform targeted supports that help autistic students thrive.

A new study from researchers at the University of Illinois Chicago reveals how the blood-brain barrier gets leakier with age, contributing to memory deficits. The study, published in Cell Reports, uncovered the molecular mechanisms behind this process and could provide new therapeutic targets to address cognitive decline earlier in the aging process.

The blood-brain barrier is a layer of cells lining the brain’s blood vessels that keep viruses, bacteria and toxins out while allowing helpful nutrients and chemicals in. A key structure of the blood-brain barrier are tight junctions that act as bridges between cells, restricting entry of molecules. A protein called occludin helps fulfill this essential role.

It’s a highly regulatable process that allows some molecules to go through and others to remain in circulation. Basically, it’s a mechanism that separates the central nervous system from everything else.”

Yulia Komarova, UIC associate professor in the department of pharmacology and regenerative medicine at the College of Medicine and senior author of the study

But like many physiological processes, the blood-brain barrier starts to malfunction as we age – it gets leakier. This can lead to memory changes as early as middle age, Komarova said. Exactly how this occurs is unclear.

In previous research, Komarova and her colleagues tested what happened if they deleted a protein called N-cadherin from the cells lining blood vessels. This made the vessels leakier in the lungs – and in the brain.

In the new study, Komarova teamed up with Leon Tai, associate professor of anatomy and cell biology in the College of Medicine, to see if this leakage had any effect on memory. Mice without functional N-cadherin could learn tasks as well as normal mice, but they quickly forgot what they learned.

A closer look at the brains of these mice showed that the issue was linked to a protein called occludin, which helps form tight junctions in the blood-brain barrier. Both aging brains and young brains lacking N-cadherin had fewer occluding junctions, resulting in a leakier barrier. Molecular experiments showed that when N-cadherin proteins on neighboring blood vessel cells interact, they trigger a signaling pathway that stabilizes occludin, helping to maintain the integrity of the blood-brain barrier.

Komarova collaborated with Dr. Jeffrey Loeb, head of neurology and rehabilitation in the College of Medicine, to examine human brain tissue from the university’s NeuroRepository collected during epilepsy surgeries. Comparing samples from younger patients (late teens to 20s) with those from middle-aged patients (40s to 50s), they found that the older group had reduced levels of both N-cadherin and occludin, mirroring the findings in mice.

The study is the first to look at how the signaling activated by N-cadherin controls organization of the tight junctions implicated in blood-brain barrier permeability, she said.

Because these deficits start to show in middle age, fairly early in the cognitive aging process, it’s not “too late in the game to start treatment,” said Komarova. Her team is now investigating if steps in the signaling pathway activated by N-cadherin could be therapeutic targets.

“This paper shows that actually there might be a much bigger therapeutic window for treatment of any age-related cognitive decline condition,” she said.

Other UIC co-authors on the paper include Quinn Lee, Wang Ching Chan, Shuangping Zhao, Harry Hailemeskel, Riya Thomas, Mohsin Zafar, Fozia Mir, Peter Toth and Kamran Avanki.

US Centers for Disease Control and Prevention Director Susan Monarez vowed to rebuild trust with the American public after the agency was the target of a deadly shooting last week, but some staff were frustrated that she didn’t offer more information on safety.

The gunman who shot nearly 200 rounds into four buildings and two security guard stands on the CDC campus Aug. 8 outlined his frustration with Covid vaccines before the rampage, according to the Georgia Bureau of Investigation. The attack occurred as medical misinformation is rampant in the US, fueling everything from political positioning to consumer purchases — and increasingly violent attacks.